Friday, October 7, 2011

The Case for the Food Reward Hypothesis of Obesity, Part II

In this post, I'll explore whether or not the scientific evidence is consistent with the predictions of the food reward hypothesis, as outlined in the last post.

Before diving in, I'd like to address the critique that the food reward concept is a tautology or relies on circular reasoning (or is not testable/falsifiable). This critique has no logical basis.The reward and palatability value of a food is not defined by its effect on energy intake or body fatness. In the research setting, food reward is measured by the ability of food or food-related stimuli to reinforce or motivate behavior (e.g., 1). In humans, palatability is measured by having a person taste a food and rate its pleasantness in a standardized, quantifiable manner, or sometimes by looking at brain activity by fMRI or related techniques (2). In rodents, it is measured by observing stereotyped facial responses to palatable and unpalatable foods, which are similar to those seen in human infants. It is not a tautology or circular reasoning to say that the reinforcing value or pleasantness of food influences food intake and body fatness. These are quantifiable concepts and as I will explain, their relationship with food intake and body fatness can be, and already has been, tested in a controlled manner.

1. Increasing the reward/palatability value of the diet should cause fat gain in animals and humans

The
most highly rewarding and palatable rodent diet I know of is the
"cafeteria diet", composed of human junk food. This diet is unmatched
among solid-food diets in its ability to cause persistent overeating and
rapid obesity in rodents, easily surpassing high-fat and high-sugar
diets, although these also cause fat gain to a lesser degree (3). Rodents will voluntarily endure extreme cold or foot
shocks to obtain this food, even when regular chow is freely available
(4, 5).

Other diets that cause marked obesity in rodents, such as
chocolate Ensure and certain purified high-fat diets, are highly
preferred to normal chow. In my own experience, rats really really like
the purified high-fat diet we feed them to make them obese. When you
put a pellet of it in their cage, they will drop everything and devour
it immediately, even if they just finished a meal of regular chow and
even if it's in the middle of the night for them (the light cycle;
they're nocturnal). If you drop a pellet of regular chow into their
cage, they will generally ignore it unless they've been food deprived.

As
I reported in a previous post, exposing humans to a similar "cafeteria
diet" causes overeating and rapid fat gain as well (6).

Some
people may object that these experiments are not properly controlled to
determine if food reward/palatability are the critical factors, i.e.,
there are multiple differences between diet conditions. For the most
part, that is true, and we will have to view these experiments as one
imperfect brush stroke in the overall painting. However, there have
been some efforts to specifically isolate the effects of
reward/palatability on obesity in rodents. In one study, investigators
added a variety of flavor-enhancing substances to standard rodent
pellets in an attempt to manipulate the diet's palatability without
affecting nutritional factors, and called this regimen the "isocafeteria
diet" (7). Here's what they
found:

It was demonstrated that the daily presentation
of a new choice of the palatable foods which composed the “isocafeteria
diet” led also to a sustained increase in food intake and to
overweight. Variety and high palatability are per se sufficient factors to overcome regulatory mechanisms.

This
effect was partially replicated by a second study that showed higher body fat gain in rats fed a nutritionally controlled diet high in fat and sugar with a variety of palatable flavorings added, compared to the same diet without flavors, although adding palatable flavors did not promote fat gain in the context of a low-fat, low-sugar diet (8). Dr. Anthony Sclafani showed that manipulating the palatability of a sweet solution (Polycose; similar to maltodextrin) using non-nutritive flavoring agents influenced fat gain in rats exposed to it (9). In baboons, adding preferred but non-nutritive flavors to standard monkey chow increased food intake and body weight (10). The investigators concluded:

These results indicate that flavored chows may be useful for producing a
nonhuman primate behavioral model of obesity and for inducing animals
to eat otherwise unpalatable diets.

Many
human studies have shown that people eat more food at a sitting if the
food is higher palatability than if it is lower palatability
(11). This is true even if
palatability is manipulated using substances that have little or no
impact on the nutritional quality of the food, including saccharin
(sweet), monosodium glutamate (savory) and herbs/spices.2. Decreasing the reward/palatability of the diet should cause fat loss in animals and humans that carry excess fat

One
of the most striking weight loss studies I've seen was conducted in
1965 and involved feeding a bland liquid diet through a dispensing straw
(12). Lean and obese
volunteers were instructed to eat as much of the liquid food as they
wanted, but they were permitted no other food. While lean volunteers
ate a normal amount of calories and maintained weight, obese volunteers
dramatically reduced their spontaneous calorie intake and lost fat
rapidly, with one man losing 200 lbs in 255 days without hunger. This
is exactly what one would expect if unpalatable/unrewarding food lowered
the biologically "defended" level of fat mass. Interestingly, the diet
was high in sugar but was otherwise very low in palatability/reward
value. Similar findings have been reported by other investigators
(13).

Monotonous,
bland liquid diets remain one of the most effective fat
loss tools in clinical practice. Similarly, diets that reduce major reward factors without deliberately calling for calorie restriction,
such as low-fat and low-carbohydrate diets, all cause fat loss even
though in some cases the diet changes that are implemented diametrically
oppose one another (14, 15). The further reward is lowered, the more effective the diet is for appetite suppression and weight loss.

Rodent studies are
consistent with those in humans. Returning rodents made obese using
palatable high-fat diets or chocolate Ensure (or by gavage overfeeding)
to ad libitum ordinary rodent chow makes them lose most of the
excess fat, although some of it is often retained
(16, 17, 18).

None of these studies are sufficiently controlled to isolate reward and/or palatability, therefore
they can not by themselves prove the hypothesis, but they are
nevertheless consistent with it.

I'm
aware of three studies that have investigated this question. In the
first, researchers found that the reinforcing value of food relative to a
non-food stimulus predicted fat gain over the next year in 7-10 year
old children (19). In the
second, the responsiveness of reward-related brain regions to imagining
palatable vs. unpalatable foods (as assessed using fMRI) predicted body
mass index (BMI) gains in adolescent girls, and this effect was modified
by gene polymorphisms in dopamine receptor genes
(20). The third study also
used fMRI to demonstrate that greater activation in reward-related brain
regions during exposure to appetizing food cues predicted greater BMI
gains over time in adolescent girls
(21).

Consistent
with other findings, these studies indicate that heightened food reward
sensitivity is a pre-existing state that predisposes to fat gain over
time in susceptible people.

4. Brain circuitry that controls reward and hedonic
processing should interact with circuits that influence food intake and
body fatness

The hypothalamus, which is the
main homeostatic regulator of body fatness, and reward/hedonic centers,
share extensive and reciprocal anatomical connections. One major
pathway runs between the nucleus accumbens (NAc), which is critical to
reward and hedonic processing, and the lateral hypothalamus (LH), which
is critical both for reward/hedonic processing and body fat homeostasis
(22). The role of the LH in
feeding and reward is illustrated by the fact that if you implant an
electrode into a rat's LH and allow the rat to self-stimulate, it will
do so compulsively as if it were administering a drug; LH stimulation
also potently increases food intake
(23). Lesioning the LH causes a
decrease in food intake and fat mass (24).

The LH
shares reciprocal connections with other hypothalamic regions important
for body fat homeostasis such as the arcuate nucleus (ARC), and thus is
likely a node for the relay and integration of information from
homeostasis and reward/hedonic systems. The ARC is a major CNS
receptor site for circulating signals of energy status, particularly
leptin but also including insulin, ghrelin, amylin, glucose and fatty
acids (25). It contains neuron
populations (POMC/CART and NPY/AgRP) that are critical for the control
of food intake and body fat mass. Manipulating the activity of these
neurons profoundly influences food intake and fat mass
(26, 27).

Reward, hedonic and homeostatic systems are in a
tightly coupled CNS circuit, suggesting that they may reciprocally
influence one another. Indeed, it is well established that homeostasis
centers influence reward and palatability circuits, and this is evident
in the fact that food tastes better when you're hungry than when you're
full ("hunger is the best sauce"). The next section will demonstrate
that reward and hedonic circuits influence homeostasis circuits as well.

5.
Manipulation of motivational and hedonic circuits in the brain (e.g.,
by lesion, drugs or genetic manipulation) should impact food intake and
body fatness

There is a tremendous amount of data
related to this question, and I don't intend this to be anywhere near a
comprehensive discussion of it. Manipulating reward or hedonic circuits can have a profound impact on food intake and body fatness. One example is
that inhibiting NAc shell neurons using a glutamate receptor antagonist
(DNQX) causes voracious feeding
(28). The mechanism involves
the stimulation of feeding centers in the LH and ARC, demonstrating the
functional importance of connections from reward/hedonic centers to
hypothalamic centers regulating food intake and body fatness
(29, 30). Similarly, chemically
lesioning the NAc shell increases weight gain in rats
(31).

Opiate signaling in the CNS is a critical component of hedonic processing. Researchers
have long recognized the ability of opiates to increase feeding, and
the ability of blocking opiate signaling to decrease feeding
(31, 32, 33). Opiate signaling in the
striatum (particularly the NAc) increases the palatability of food, and
this effect depends mostly on the mu opioid receptor subtype
(34, 35). The mu opioid receptor
blocker naloxone specifically decreases the palatability of food and the
consumption of palatable food in rats and humans, but has little impact
on the intake of less palatable food
(36, 37, 38). Mice that lack the mu
opioid receptor gene are lean and resistant to diet-induced obesity, suggesting that opioid-mediated food palatability may be a major part of the reason rodents become obese on refined high-fat diets
(39). Activating opioid
signaling in the striatum does not increase
the amount a rodent will work for food, does not increase meal
frequency, and does not reinforce behavior, thus striatal opioids
regulate hedonic processing (liking) without affecting reward (wanting)
(40).

It has
been demonstrated many times in the scientific literature and in my own
hands that rats will eat a substantial amount of palatable food even
after they have already eaten less palatable food to fullness
(41). This is the "dessert
effect"-- you've just finished a large meal and you're stuffed, but you
manage to "make room" for another 200 calories when the cake rolls
around. This seems to be related to opioid signaling, as the activation
of this system in the striatum increases both the liking of foods and
meal size (42).

Dopamine
is critically involved in reward functions, and it turns out to be a
major regulator of food intake and body fatness as well. Injecting
dopamine into the brain reduces food intake, and the primary site of
action appears to be in the LH
(43). Dopamine signaling in the
striatum regulates the motivation to obtain food, but not the enjoyment
or consumption of food that is readily accessible
(44). Thus, in the striatum it
impacts motivation/reward (wanting) but not palatability (liking).

Drugs
that activate certain dopamine receptors can cause compulsive
overeating of palatable foods and weight gain
(45). However, the dopamine
system is complex, involving multiple receptor subtypes that have
different functions in different brain regions, and different drugs
affect these subtypes differently. The dopamine D2 receptor in
particular seems to be involved in food intake and body fatness. The D2
receptor activating drug bromocriptine causes fat loss in a variety of
animal models of obesity, including humans in some studies
(46). Obesity is associated
with reduced D2 receptor density in the striatum, and there is evidence
that reduced striatal D2 receptors can precede the development of obesity
(47). There is also evidence in rodents that chronic exposure to highly palatable food can reduce D2 receptor density in the striatum (48), suggesting that exposure to hyperpalatable foods, in addition to genetics (discussed below), can lead to an obesity-promoting pattern of D2 receptor expression in the brain. This is part of a broader pattern of addiction-like changes that develop in the brains of animals chronically exposed to hyper-palatable/hyper-rewarding food.

If
the effects of opioid and dopamine signaling on palatability and reward
truly influence food intake and body fatness, then drugs that impact
these systems should be able to cause fat loss in humans. Such a drug
exists-- it's called Contrave, and it is a combination of naltrexone (an
opioid receptor blocker that acts mostly at mu and kappa receptors) and bupropion (dopamine-norepinephrine
re-uptake inhibitor). Contrave has shown effectiveness as a fat loss
drug in humans, although side effects have prevented FDA approval(49).
The proposed mechanism of this drug is via the indirect activation of
POMC cells in the ARC, again suggesting that reward/hedonic circuits
influence those that regulate body fatness.

One of the most interesting links between reward/hedonic circuits and hypothalamic circuits is via
endocannabinoid signaling. It has been known for some time that
marijuana increases the consumption of palatable foods and causes weight
gain if smoked frequently enough
(50). Today, we know that
endocannabinoid signaling is intimately involved in hedonic and reward
circuitry. Marijuana acts principally via the CB1 receptor
(51). Mice lacking the CB1 receptor gene CNR1 are lean and resistant to
diet-induced obesity (52). The CB1 receptor blocker Rimonabant is an effective fat loss drug in humans, and
its effect appears to occur mostly if not exclusively in the brain
(53, 54). Rimonabant is basically
"reverse marijuana". Perhaps not surprisingly, it was pulled from the
market by the FDA due to negative psychological side effects.

It
is no coincidence that two of the most effective fat loss drugs
developed in recent history, Contrave and Rimonabant, both target reward
and hedonic centers in the brain.

Each person on this earth carries a unique combination of gene variants, and in some cases these influence physical characteristics and the response to environmental factors. Some of these variants are within dopamine receptor genes, and thus have the potential to influence food reward. Several studies have shown that polymorphisms of the D2 dopamine receptor associate with the risk of drug addiction, gambling addiction, and obesity (55, 56, 57, 58, 59, 60). Polymorphisms in other genes that influence dopamine signaling, including the D4 dopamine receptor, the dopamine re-uptake transporter, and catechol-O-methyltransferase, have also been found to associate with obesity risk (61, 62, 63, 64).

Polymorphisms in the CB1 cannabinoid receptor gene CNR1 also associate with body fatness (65, 66). This is consistent with the fact that the CB1 receptor knockout mouse is resistant to diet-induced obesity, and the CB1 blocking drug Rimonabant reduces body fatness in humans (67).

I have not come across any reports of opioid receptor gene polymorphism frequency in obesity.

These findings support the hypothesis that reward and hedonic circuits in the CNS influence body fatness, and that the pre-existing characteristics of these circuits can explain differences in the response to rewarding stimuli, and differences in body fatness, in the general population.

7. On a cultural level, obesity prevalence should track with changes in
the reward/palatability value of prevailing diet patterns

The evidence in this category is the least well controlled, since many things have changed during the development of the "obesity epidemic". However, for the hypothesis to be convincing, at a minimum it has to be consistent with how diets in most cultures have changed as obesity has increased in recent years.

The obesity epidemic in the United States has paralleled a significant shift in food culture. Here are a few examples to illustrate the trends (68). In the last 50 years:

Between-meal snacks/drinks, particularly processed snacks and soda, have more than doubled (69)

These changes outline a broader trend: the shift from simpler home-cooked food to professionally engineered/processed food designed to maximize palatability and reward. Food manufacturers go to great lengths to accomplish this goal: hiring "flavorists" to optimize mixtures of chemical aromas, manipulating fat, salt, sugar and glutamate content, and systematically testing different permutations on focus groups before marketing.

Similar trends are apparent in all affluent nations as the food chain has become increasingly commercialized and gradually displaced traditional food culture, and invariably this has been accompanied by increased body fatness on a population level.

That's not to say that commercial food is responsible for all obesity. Obesity has been documented for thousands of years, if not longer, including in certain cultures that only had access to traditional ingredients (e.g., Polynesian islanders). However, in these cases (including Europe before industrialization), obesity was mostly restricted to affluent individuals who benefited from skilled chefs and choice ingredients, as well as a sedentary lifestyle.

Some people have brought up the examples of France and India as challenges to the food reward hypothesis, stating that both have a tradition of delicious food. That, of course, is true. However, it's important to remember that most people traditionally didn't eat foie gras and fatty spiced curries every day, and food that you eat in a restaurant or as a tourist doesn't necessarily represent peoples' day-to-day food choices. In France, which I can speak for because I spent a significant chunk of my life there, most meals are composed of relatively simple, fresh, home-cooked food. This is particularly true for the older generations. The food is not low in fat, or low in animal fat. It tastes good, but it isn't extravagant. Traditionally, people rarely ate at restaurants, which were expensive and considered a special treat. As the food system has industrialized, and commercial food has increasingly replaced home cooking, the prevalence of obesity has increased.

I'm not as familiar with traditional Indian food, and I don't want to pose as an expert here, but I'm quite confident that what we see in restaurants and cookbooks in the US is not what the average Indian person was eating 50 years ago, and for the most part still not today. The traditional Indian diet, before industrialization, differed by region but was generally very low in fat and relied heavily on plain starch foods such as rice, millet and wheat. This was supplemented with more exciting dishes based on legumes, vegetables, dairy and occasionally meat. But my understanding is that, for an ordinary meal, these were small portions compared to the plain starches that formed the backbone of the diet. I doubt the average Indian person 50 years ago was making complex dishes using liberal quantities of ghee and a dozen spices for dinner every night, or deep frying things. Spices and ghee aren't free and cooking like that takes time, skill and special equipment-- is it a priority if you don't have much disposable income?

As India has industrialized, and the diet has become more diverse, more fatty, more refined and more commercialized, obesity throughout the country has increased (particularly abdominal obesity), and India now has a serious diabetes and coronary heart disease problem on its hands.

Conclusion

If you made it this far, you're a hero! As you have seen, a number of mutually buttressing lines of evidence, including controlled diet studies, observational studies, neuroscience, pharmacology and genetics, support the hypothesis that food reward and palatability influence food intake and body fatness. It's not every day that you come across an idea in the diet-health literature that is consistently supported by so many independent lines of inquiry. This hypothesis isn't very sexy, which is one reason why it hasn't gained as much traction with the public as certain other ideas, but I'm not too concerned about that. I just want to understand what causes obesity, and this hypothesis has a lot of explanatory power.

The degree to which food reward and palatability have driven the modern obesity epidemic remains open to interpretation. However, in 2011, the
evidence has accumulated to the point where it is clear that they
play a role. I side with modern food reward researchers in thinking it is a
major factor, although there are certainly others.

69 comments:

Stephen this is a fantastic overview... I think you have drawn the various strings of evidence together in a compelling way.

I would like to ask though, apart from eating unpalatable food, how does one lose weight... I understand that it is effective for weight loss, but how does someone live their life eating food without reward/flavour/palatability?

Also, you mention a number of times that once these animals are obese, if they lose weight they never lose it all... does this mean there is no hope for those of us that have over indulged in hyper palatable foods and is now overweight?

Have we over stimulated the reward centres in our brains so much and reduced D2 receptor densities to the point we will always be pushed towards holding excess weight.

I guess my question is, what you are describing is in essence changes to regulatory/reward systems due to over stimulation due to diet choices, and one would expect the system to reverse if this stimulation is removed/reversed, but is there evidence that the damage to the system is irreversible?

This is important, as people struggling with weight loss need to know what they are capable of achieving, as the very systems you are describing being involved with weight loss/gain, would suggest that if people feel they are failing (when in fact they just never had a chance of EVER getting back to normal weight), there would be an increased chance for these people to seek "reward" through food to overcome these feelings of failure, thereby negating any benefit they had achieved previously?

You have nice assumptions but fat intake is needed to our body. The question is - what internal mechanism regulates _balanced_ food intake and how it is broken. I suspect\ guess that the reason is sugar in all forms.

or you could say that our body can handle very different food intake regimes (high fat + high carb\ low carb + high protein \ all vegs etc) but its not accustomed to quick changes in food intake regime.

Our brain could quickly decide another food intake regime (in response to high stimulation from ads etc), but body is still function in old regime (takes time to change)

"I doubt the average Indian person 50 years ago was making complex dishes using liberal quantities of ghee and a dozen spices for dinner every night"

I'm often jealous of my Indian co-workers who have stay-at-home wives and eat these elaborate dishes for lunch every single day. But yes, you are probably right about the ghee, particularly since cheap fatty fake ghee is available in the pint-size for pennies.

But that's my issue with fermented grains and other elaborate traditional grain/dairy preparations- they are from an era where women spent a lot of time in the kitchen.

terrific write-up, as usual. I love this line, and feel that it is a key to help lay people get the gist if you will: "the shift from simpler home-cooked food to professionally engineered/processed food designed to maximize palatability and reward." Also I like how you cite that plain potato consumption has decreased while processed potato consumption has increased. Fantastic point; reminds me of how studies pointing to meat as unhealthy will lump sausage-topped pizza with a grass-fed steak.

I think that food reward/palatability probably play a major role in obesity. Lord knows I went through some serious withdrawal when I stopped eating sugary baked goods. Still crave them to this day. BUT, as a prescription for obesity, well, eating plain food just isn't very appealing. Even though obesity runs in my family and I may have some of those polymorphisms you discuss, I'm not going to stop eating yummy food and go to a bland food diet to make sure I never get obese. Maybe the low carb paleo diet works through this effect, but I still think eating less carbs makes me less hungry, especially between meals. Maybe that's due to the reward of the carbs I was eating, I don't know, but if it works don't fix it.

Stephan, the conflation of high reward with high palatability still offers no explanatory power to those of us who have lost substantial weight and have kept it off with low reward, high palatability diets. Our experience asks that these things be teased apart. Meanwhile you seem to be unnecessarily recommending bland diets to many who need not suffer through them.

Stephan, I do not understand how you have addressed the tautology argument as regards reward (palatability is not the issue here.)

1) You said, "The reward ... value of a food is not defined by its effect on energy intake..."

2) You said, "Food reward is measured by the ability of food or food-related stimuli to reinforce or motivate behavior."

so either:

3a) The behavior that is reinforced by food reward does involve energy intake which makes #1 false or

3b) The behavior that is reinforced by food reward is not related to energy intake. If so, what could this behavior you describe in #2 possibly be? (The reference that you cite involves palatability and not reward.)

Until someone comes up with a bullet-proof, simple, definition of palatable/high reward, we are going to keep going around and around in circles. So long as those terms remain subjective, we will have people pipe in to say, wait a minute, my diet is highly rewarding/palatable but I'm losing weight.

Steve, I have been reading you blog for a month now, and regarding the palatability concept-- I just keep thinking about a movie called Blood into Wine with Tool lead singer Maynard James Keenan. The psychology of taste is so wonderful and complex, and is influenced by so many things such as subtle flavors and in humans, price, eyesight, and context too. I am glad you are exploring the roots of where it happens, how it happens, and how it's influenced. Keep up the excellent work!

If you fed people, or rodents, say 10% or so of their calories as highly palatable 'cafeteria' food, do you think that amount would cause overeating of the less palatable food in their diet, due to a rise in the set-point? Seth Roberts suggests that even small amounts of hyper-palatable food can have this effect.

Also, from your experience, do the French consume much wheat while cooking at home?

Those commenters who keep doubting this hypothesis because they lost or controlled body fatness using low-carb or paleo perhaps don't realize that they are the lucky ones...their genetic variation allows them to respond readily to phase one of reducing reward: remove the junk.

Your foods remain very tasty, but they lack the engineering that makes them uniquely able to promote obesity.

I would like to provide some personal insights from the other end of the genetic spectrum.

Even when devoutly following zero-carb or paleo diets, I have had great difficulty controlling my intake. And I mean devout; my devotion to low-carb/paleo included a years-long phase of making my own pemmican from scratch. If you've ever rendered 50 pounds of suet in a day you will have some inkling of how dedicated I was!

I know that I have OCD tendencies in many areas of my life and have struggled to break habits unrelated to eating. After reading Stephan's posts, I became self-aware that my response to non-food stimuli is deeply embedded into my response to food as well.

I have learned from hard experience that (for me), overcoming ingrained habit requires total abstention from the stimuli. Fortunately, the compulsions drop off after a couple weeks, and disappear after about 3 months. With recent experimentation, I can say the same thing applies to my food compulsions.

Does a bland-food diet sound unappealing? It depends upon your perspective. I would never recommend the level of blandness I now maintain to anyone as a first step...but then, neither did Stephan. But if you have never suffered from uncontrolled eating/gorging brought on by tasty triggers (even paleo ones) then you cannot appreciate the profound relief that one can receive from being free of these uncontrollable behaviors.

It still takes willpower for me. But my breakthrough came in learning when to apply the willpower. I apply it when it is easy: BEFORE I take the first bite and can walk away. Trying to apply it after the first bite is, for those who are genetically susceptible to the cascade of effects in the brain, simply impossible.

I'm not dramatically overweight; just struggling with the classic "20 extra pounds." My weight is not melting away on this diet. It has finally quit increasing, though, and is very very slowly creeping downward. Perhaps Stephan has provided the answer to this frustration above; I too hope that my receptors will remodel with the passage of stimulant-free time.

I've gone on too long. This is my own "sample of one" that I hope will help explain to some of the commenters something they can't understand because it is too far outside their personal experience.

Scott W

PS - Thank you Stephan for your tireless work in this area. It has made a difference in people's lives. Certainly it has in mine.

When the Taubes/Guynet controversy first blew up on this blog, I weighed in with my anecdotal experience and Native Hawaiian traditional observations regarding poi used by Native Hawaiian women who specifically desired to get fat by consuming large amounts of poi.

I posited that this ran counter to the food reward theory, and attributed it to Taubes' argument connecting chronic blood sugar elevation due to excessive carbohydrate consumption.

Yet, after reading and re-reading these Food Reward hypothesis posts here and elsewhere, I now think that in fact, excess poi consumption leading to obesity can certainly fit in with the Food Reward Hypothesis.

Poi is, afterall, to the Western palate used to processed sugars, and artificial sweeteners "bland."

But what it really is, is a primitive form of "processed" food that certainly increases it's food reward value.

Back when I was quasi-vegetarian and consumed up to a pound of poi a day, I developed what can be described as an addictive craving for it.

I would buy a 1 lb. bag and eat it throughout the course of the day, usually starting off with a half pound of it for breakfast, in conjunction with a banana. Than I would snack on the poi throughout the day at regular intervals.

When eating like this, I also experienced the wild roller coaster levels of energy, and probably had wildly fluctuating blood sugar levels (I never measured it with a blood glucose meter, I can only go by memory here)...when it would get really low, I'd get that shaky, nauseous feeling until I ate something (usually more poi, plus whatever other foods I was regularly eating then) - a common pre-diabetic/diabetic symptom.

From an anecdotal experience, this does seem to corroborate the Taubes' theory of simple carbohydrates driving obesity...but when considering the food reward hypothesis, could it be that the blood sugar/energy fluctuations simply be a "side effect" here and not the primary driver?

As taro paste is pounded and fermented, it turns the taro into something so easily digested that it causes a blood sugar spike that triggers the food reward response?

There's also the mildly sour taste to fermented foods. I find that taste highly rewardable. So much so that I could live off of soured quinoa exclusively. When just reduced in phytate without reaching that sour taste, I can't really eat much at all. And that amount needs fat, meat and salt. When making fermented corn drinks, the bubbly can be rewarding too. Isn't poi traditionally "done" when it gets a little bubbly?

I've lost interest in trying to lose weight or whatever. I just eat nutritious "peasant food" and leave it at that. It's satisfying until I'm full. That's good enough for me. I have better things to be worrying about.

As has been discussed ad nauseam, there is bound to be overlap between the two (dear average LCHF proponent, your highly palatable diet of bacon/eggs is much lower reward (from a dopamine signaling standpoint) than you think!)). But for the purpose of evaluating the hypothesis, it's helpful to delineate.

I think part of the frustration lies in our natural "Well Duh" response to mechanism [1]. We all realize that dressing up foods with salt/fat/sugar/MSG--even paleo approved foods (note: the confection is not always the sum of its parts from a FR perspective, Dr. Harris may be right that these Paleo Frankensteins are NADs in their own right)--will usually result in excessive eating due to confounding of the normal satiation signals (hat tip to J. Stanton at gnolls.org for his "Why Are We Hungry" series - fantastic). I think this intuit is what's driving some of the accusations that Stephan's reasoning is circular.

That said, the elephant in the room is the evidence Stephan is presenting with respect to mechanism [2].

Stephan seems to be crying out:

"IT'S THE BRAIN, NOT THE CALORIES [stupid]"

Specifically, there appears to be a connection between dopamine (reward) and leptin (fat setpoint).

Here are two pubmed abstracts discussing the interconnected nature of dopamine and leptin:

I think we can all agree that leptin resistance is the primary driver of fat gain and obesity. Based on the evidence put forth by Stephan, I think we should also give fair trial to the idea that the dopamine/reward and leptin/obesity pathways in the brain are intertwined.

We know that the "calorie burn" model of exercise is bogus, yet we still see a correlation between leanness and activity. Peripheral insulin sensitivity aside, perhaps we've been overlooking the effect of exercise on the brain?

I can't speak for any-one else who commented, but when I criticised your hypothesis for circularity I wasn't claiming that you defined food reward in terms of causing body fatness and said 'high reward food [food which causes fatness] causes fatness.'

Rather, I took your hypothesis to be 'high reward food [food which strongly reinforces], increases eating and so increases fatness.' But how were you proposing to identify in your experiment how strongly foods reinforced behaviour? If by looking at how much the people ate afterwards, then this wouldn't seem very informative, since you would indeed be testing whether eating foods which lead to you eating more, lead to eating more and so to increase of body weight. (I note from the link you posted that one could determined reward by seeing how much work people are willing to do to gain food, but that doesn't seem any more informative). This wouldn't invalidate the food reward hypothesis of course, but it would render your test and the dietary prescription which it vindicates (eat food which leads to you eating less) uninteresting. Interesting things can still be found out about food reward of course- like the things you've listed above about genetic differences and the particular neurological elements that influence food reward, but your proposed test didn't seem to gain a handle on any of these things. Rather your test and dietary prescription seemed to rely on coupling reward with palatability, which is obviously problematic. You seem to do the same thing in your first paragraph, giving examples of palatability. I'm still not clear how “It is not a tautology or circular reasoning to say that the reinforcing value... of food influences [reinforces] food intake.”

On weight-reducing drugs, there is also Sibutramine. To quote Wiki "Sibutramine is a neurotransmitter reuptake inhibitor that reduces the reuptake of serotonin (by 53%), norepinephrine (by 54%), and dopamine (by 16%), thereby increasing the levels of these substances in synaptic clefts and helping enhance satiety; the serotonergic action, in particular, is thought to influence appetite."

Stephan, as uual this very well done. Over the course of this series I’ve persuaded of the following:

-Food reward is a biologically meaningful concept.

-Food reward is a powerful determinant of caloric intake.

-Processed foods that have been engineered to maximize food reward are likely THE major triggering factor behind the recent obesity epidemic.

-Palatability (or 'liking') is a major factor in determining food reward.

-A diet featuring a limited variety of gently cooked whole foods with little added sugar/fat/salt will be for many a useful strategy for combating obesity.

However, I (and other commenters as well) am having a problem with the contention that reward and palatability must always travel together. You wrote the following:

'In France, which I can speak for because I spent a significant chunk of my life there, most meals are composed of relatively simple, fresh, home-cooked food. This is particularly true for the older generations. The food is not low in fat, or low in animal fat. It tastes good, but it isn't extravagant.'

Right, but is the traditional French diet actually less tasty than a diet of Hot Pockets and Coke? Are the French getting less pleasure out of their meals than Americans on the SAD do?

I would submit not.

I also thinking about the differences between the French and American diets yields interesting insights on the concept of 'blandness'. Are baguettes more bland than Wonder bread? Is Camembert more bland than Velveeta? No. And yet Wonder bread and Velveeta seem to be more associated with obesity.

I find the evidence pursuasive but I'm still a little bothered by the lone "fat" kitavan who had spent some time off island.

I wish we knew more about this individual.

If person who was lean and fit on a native diet adopted a high reward obesity promoting diet and did gain weight, what is it telling us that the weight was not lost upon returning to the native diet and lifestyle?

In the liquid bland diet the weight loss was swift...native diet would no doubt be more rewarding but still it's strange that obesity persisted despite the passage of time. There was no timeframe given if I recall correctly but I'd have to wonder if a person who had spent a considerable amount of time off island and had only recently returned would "qualify" as part of the population studied.

So assuminng at least a period of several months had passed during which diet was more or less optimal/low stimulation, activity level was presumably moderately active as per the rest of the population, wake/sleep cycles were in order etc and so on...but still fat? Not just heaviER than the average Kitavan but actually overweight.

Maybe I'm simple, but a simple thought keeps occurring to me in this "food palatability" argument. It has to do with the body essentially BEING or quickly BECOMING what it eats.

Take for instance our yearly move to the lake every summer, when I was young. There was a LOT of iron in the water at the cabin and it tasted horrible. More horrible than you can imagine. Also made the clothes orange if one didn't use a water softener. BUT!!! We knew from experience that in 4 days, we wouldn't taste the water anymore. Not at all. And we didn't.

Aside from the science of it (for which we are indebted to Taubes' research of the research), isn't "food palatability" pretty much THAT? We are what we eat? (Sorry, I hate that cliche formulation...) But the thought keeps coming to me that What if it's as simple as that? Just as an alcoholic doesn't feel RIGHT until he has his alcohol, and a carb junkie experiences relief upon consuming his carbs.

"Food palatability" -- WHAT?!? That's a total aside from figuring out what is good for us.

Steve, good article. But you need to address the following comments and questions:

1. dim sum massacre is the traditional French diet actually less tasty than a diet of Hot Pockets and Coke? Are the French getting less pleasure out of their meals than Americans on the SAD do?

2. if the answer is NO, as I agree with "dim sum massacre", then you need to revise your hypothesis.If the answer YES, how do you measure it?

3. there is still a big link to or question on carbohydrates in your hypothesis, based on your cafeteria diet. Typical cafeteria diet is very high in simple sugars/carbs. May be it's the simple over-processed carbohydrates after all and not the taste/reward that is a problem. How do you solve this? Can you isolate the effect of carbs on palatability/reward from fat and protein?

4. can humans eat unlimited amount of fat and protein + spices to make it super tasty and get fat? why do we always need carbs to gain weight? Is it something only specific to carbs? are simple processed carbs just more palatable/rewarding and addictive? Does your hypothesis address this?

5. May be we need to combine carbohydrates theory with palatability theory. Processed simple Carbs are tasty but provide little nutrients and no long lasting satiation, and possibly are uniquely addictive to the brain (may be even more addictive if we mix simple carbs with fat), thats why we overeat them. Protein and fat are also tasty, but provide lots of nutrients and long term satisfaction of hunger.

This is the annoying thing with detractors from any theory. They take away from its validity by stating some simplistic contradiction, without taking into account any other factors. Sure you can say food reward might be similar with home cooked french cuisine and hot pockets/coke, but you keep forgetting the nutritive (not sure if that's a word) value of these foods. If you're getting malnourished as a result of your food, you will continue to have cravings to satisfy it. WHile if if you are eating a low reward and a nutrient dense diet, then obviously you will be arming yourself against more than one possible foe. Its pretty obvious that nutrition-in regards to obesity this time around- functions on multiple modalities, excluding nutrient composition from food reward seems foolish and myopic(near-sighted) in my opinion.

I think the take home message is that both palatability and reward are individual. We all have different foods that give us high reward regardless of palatability. If weight loss is an issue it may be an idea to avoid those individual foods that make you want to eat more even when not hungry. For some people this is doughnuts, cookies or cake and for some like me, it's all those plus rice, maybe because eating rice always puts me in the mind of Chinese fried rice! Potatoes for me on the other hand, are palateable but provide the most satiety of any other food I eat bar none and all without leading me to wanting to eat more of them. In my bingieng days when I would hop over to a fast food outlet, even the fries always seemed like a mild annoyance I had to get through for the prize that was the burger (high reward wheat with the palatability of the meat).

I don't think a bland diet is necessary if you are avoiding the foods that give YOU the most reward.

To your points, I do wish Stephan would at least address the role of satiation/satiety with respect to the big picture of weight gain within the context of FR. From an experimental perspective, it makes sense that reward can be considered in isolation. However, from a practical perspective, satiation factors seem inextricable. Food reward will never *quite* operate the same as pure drug reward.

For example, for me, plain chicken breast quickly rises in palatability when butter is added, but food reward remains constant.

It doesn't seem far-fetched to speculate that satiation factors may play a role in how acutely our "FR brain" lights up--and therefore downregulates long term--in response to various foods.

"I don't think a bland diet is necessary if you are avoiding the foods that give YOU the most reward." - A.C.

+1, I think this is the point that many are missing. As Stephan has said, only in the most extreme cases will an uber extreme bland diet be necessary. For the average person looking to lose weight, a few simple tweaks may be the minimum effective dose.

Thanks Stephan- I can grasp FR better when reward=palatability as you suggests it does in this post by merging them with a slash mark for the most part… what I am missing is how this is different from all the other weight loss programs. I have seen folks lose weight (lower fat set-point) by intentional calorie restriction alone (portion control w/weight watchers). Is this the same thing as calorie restriction that happens spontaneously when food does not taste as good or because it carries fewer calories per gram if you cut out some fat to increase the “blandness factor? Other diets (low fat, low carb) could work because the reduced choice causes a forced calorie restriction and then a lower set point. The rodent studies are interesting- can we measure the same responses in humans? True, many people will eat dessert (rewarding food) when already full, but can we measure/calculate/prove what is driving that decision to take in extra calories?

Also, I am still confused about what we should eat if we accept that FR explains our modern problem w/obesity… if cutting the processed food is all that is needed that seems straightforward, but I don't think that is what you are saying:

On French food: “most meals are composed of relatively simple, fresh, home-cooked food. This is particularly true for the older generations. The food is not low in fat, or low in animal fat. It tastes good, but it isn't extravagant.”

“I doubt the average Indian person 50 years ago was making complex dishes using liberal quantities of ghee and a dozen spices for dinner every night”

It sounds like French home-cooked food w/fat may be OK (not overly rewarding?), but Indian home-cooked food w/fat is not OK (too rewarding?)And in general it is not enough to avoid the obvious junk food, but we should eat like traditional poor Indians:

“The traditional Indian diet, before industrialization, differed by region but was generally very low in fat and relied heavily on plain starch foods such as rice, millet and wheat”

One last thing I have wondered: can FR theory explain fat babies/toddlers?

@dsm- thanks for your replies from part 1, I got behind on reading comments, but I appreciate you trying to help me understand. Separating FR and palatability seems more intuitive to me if we take in to account nutritional content as suggested above (although I do not think this is part of Stephan’s theory unless I missed it). So maybe a chip is tasty AND over-stimualtes reward centers because it lacks nutrients- foie gras is tasty ,but not overly rewarding because it is nutritious so we are not driven to seek more food after eating it ??

James_M,Your comments are well put, especially with regard to the importance of satiety/satiation, the idea of a ‘dopamine/leptin axis’, and the difference between results from controlled lab experiments and their practical application.

Sandra,It seems to me that fois gras is not overly rewarding primarily because it induces a high degree of satiety. If someone made the decision to purposely overeat large portions of fois on a daily basis, it would likely result in the same sort of dopamine overstimulation that one would get from overeating potato chips. It’s just that fois is actually pretty hard to overeat.

Nutritive value probably does play a part in food reward, since a diet that is nutrient poor may also tend to be non-satiating. But it's not a simple correlation. As Kurt Harris has noted, it’s entirely possible to take nutrient rich 'paleo' foods and engineer them to be high-reward.

Stephen - Isn't the rise of mass produced, hyper-palatable food also correlated with food becoming cheaper, not just in terms of direct cost, but time to prepare? Someone is much more likely to buy a cookie from a vending machine when bored, then they are to go home and make cookies from scratch. Manufactured and packaged food make treats more accessible, regardless of whether or not they are more rewarding. This idea, also, to me explains the French paradox even as it applies to food reward: I spent a year living in France and found that it was culturally less acceptable to snack in public and in the workplace, so treats were just not as accessible as in my US workplace where free donuts and brownies are left around every afternoon on a regular basis. It doesn't matter how rewarding the food is if it takes too much effort to get.

Do you feel the factor of cost-of-preparation confounds food reward?

The following paper discusses the subject at length: http://www.ers.usda.gov/publications/efan04004/efan04004b.pdf

Actually, ghee, was a staple of the traditional cooking in India, especially villages, and has been virtually replaced by vegetable oils. Ghee is incredibly expensive nowadays and villagers, let alone city-dwellers, have shifted to the 'cheaper' vegetable oils to cook in.

For Hindus, the cow is considered holy and ghee is found in countless of their religious texts, meaning it's usage ingrained in their psyche.

They also enjoyed plenty of dhai or yoghurt and butter and ate them probably daily. For the yogi, it was the preferred food of choice to start the day with.

Considering they were and are farmers, dairy-based products go way back in their culture.

But, interestingly, to contribute to Steve's point, yogis avoided such as garlic, onions, and chillies, because they were too stimulating.

The Pathans of Afghanistan are no different in regards to dairy, except they indulged in heavy meat-eating, and cook their kabobs in fat as well.

"Consistent with other findings, these studies indicate that heightened food reward sensitivity is a pre-existing state that predisposes to fat gain over time in susceptible people."

So when one over-indulges the senses, the ability to seek pleasure from these things decreases, thus one seeks to find other, what you term, "over-stimulating" things to create a reward value. So essentially, one is saying gluttony is one of the seven deadly sins that causes obesity...

Are on of these studies long-term? For example, what if I continue over the years to feed a person the same 'cafeteria' food that is highly-stimulating? It may just act just like the 'bland' food in the long run, because the brain would ultimately adjust to this 'sensation' of 'stimulation' and the food would no longer be rewarding...

"Rodent studies are consistent with those in humans. Returning rodents made obese using palatable high-fat diets or chocolate Ensure (or by gavage overfeeding) to ad libitum ordinary rodent chow makes them lose most of the excess fat, although some of it is often retained (16, 17, 18)."

How long were these rats obese?One once become obese, a shift back to a non-rewarding diet does not necessarily return the body weight back to normal, i.e. fat gain still remains. What this seems to imply is that once your obese, especially for a long time, it isn't so simply...

"The further reward is lowered, the more effective the diet is for appetite suppression and weight loss."

That does really address the issue, which is what causes the brain to assign reward value to a particular food.

“In the research setting, food reward is measured by the ability of food or food-related stimuli to reinforce or motivate behavior (e.g., 1). In humans, palatability is measured by having a person taste a food and rate its pleasantness in a standardized, quantifiable manner, or sometimes by looking at brain activity by fMRI or related techniques (2).”

I think it would be extremely useful to keep these two concepts distinct. Food reward in this sense is the outcome of a process which may be outside our conscious control, indeed may be completely unknown to us (except for a few researchers). Palatability, however, lies much closer to the surface, and it seems reasonable that, other things being equal, one might eat more of a more palatable than of a less palatable food. Nevertheless, one would expect sateity to kick in in both cases, and one would expect hunger to be deferred after the larger meal, and no road to obesity.

The two puzzles to me are a) why do some foods seem to bypasss the sateity regulator ? and b) why and how are some foods more habit-forming than others ? If a manufacturer could create a habit-forming non-satiating food he could expect commmercial success.

However, I have seen completely contradictory reasoning around the blogs, along the lines of: 1) Non-satieting food doesn´t give the gut the nutrients it needs, so the body' response is to eat more (and more). And 2) Habit-forming food is habit-forming because it is nutrient dense, so that our body wants to keep going back to it.

The only way to reconcile these two is to posit the existence of foods which fool the body into thinking they are nutricious while at the same time the body knows they are lacking in nutrients. This means we have at least two processes involved, which can interact in a dysfunctional way. I propose we have a choosing brain process based on look, smell, taste, and an evaluation gut process based on actual digestive results. The dysfunctional food reward process becomes:1.gut to brain – we need some more nutrients2.brain – This (fill in anti-food of choice) looks, smells and tastes nutricious, I'll eat it3.gut to brain – we're still short on nutrients4.brain – better eat some more of the same5.gut to brain - we're still short on nutrientsetc ad nauseam (literally)

How Paleo / Atkins / WAPF etc work then is simply that the foods that are eaten are actually nutricious and trigger sateity at the right point.

How Shangri-La etc work is that nutrients are applied without the look, smell, taste evaluation being applied.

I would like to add my observation about processed food in FR.I live in Stockholm, Sweden. Here we luckily dont have much child obesity (yet) but I have noticed that within my circle of friends and relatives a few kids are way more chubby than they ought to be at age 7 to 11 or so.

They eat at home or at school, except possibly once at McDonalds during the weekend. School food here these days are usually "homemade" in the school kitchen, so not too industrialised. Its actually proper food except they use seed oils for practical reasons. Very little fat, no msg or sugar.At school the kids can choose to drink milk, or water only.

But heres the thing, I have observed that the chubby kids are without exception served sugary drinks at home, either lemonade or chocolate-sugar in milk.

I also see slim kids that drinks a lot of sugar at home, but those usually do a lot of sports.

So for kids in Sweden, no processed food is required for chubbiness, sugar alone will do the trick.

It is also a bit less less confusing for the rest of us to know whom you are addressing.

Can we get rid of the acronyms like "NADs" and such... it's like a middle-man created by the person writing "NADs" to save time (and maybe write a book with made-up acronyms), but wastes thousands of time for others to decode each time and for those who are new, and also accredited, it's obnoxious and culty. ...

We've known for years that glutens grains are addictive by activating opioid brain receptor sites. This makes them especially rewarding, even though grains, on their own, are rather bland. For example, no one eats just pasta alone -- it's always drenched with a delicious sauce to make it palatable.

Plain starches may not as highly palatable as some processed foods, but they are by no means unpalatable to the point of requiring sauces to be palatable, at least to people like me.

I used to frequently eat pasta and oats alone. I still eat instant rice alone on an almost daily basis, and I frequently eat bread alone while traveling. Occasionally, I buy potatoes and corn tortillas and eat those alone (after cooking or heating, respectively). And I've seen plenty of other people do the same thing.

Makes sense..when I'm on a diet I fail as I end up not eating enough. Unless I like a food, there's no point me eating. Apparently I don't lose weight as I'm not eating enough calories (not that I eat that many anyway but my body is an idiot and won't respond to anything I do).

Just curious if you have read this study and if so, what your thoughts are on it?

http://www.ncbi.nlm.nih.gov/pubmed/17668074

I've recently come to the conclusion that I'm fructose intolerant but I'm having a hell of a time cleaning it completely from my diet. After a few days of "being good", I inevitably break down and get a chocolate bar or something else, from one of the six convenience places located not two blocks from my place. I think I need to check into a clinic for sweet-aholics anonymous.

The main defect in the Food Reword theory is the lack of explanation why two individuals affected differently by similar food, like two friends who went on vacation together , eat mostly salads, one lost weight, another gained some; G.T.'s example of emaciated malnourished child and obese mother; a lot of obese individuals who diligently follow calorie-counting recommendation and unable to loose or even gaining weight; an approaching menopause women who had been always able to keep her weight down by eating less, exercising more until she reached 45.There are different reasons why people are fat. Food Reword is explaining behavior a narrow group of foodoholics, mostly Americans, and not world-wide applied. Not all of fat people are binge-eaters, gluttons or even find cafeteria food attractive. Low-carb theory could be applied to more people in a wider range of behaviors and cultures, even foodoholics could be helped.

Low carb suffers from the same problem. Why do some people lose fat after reducing carbohydrate, and others gain fat? There is always variability due to individual differences. Variability in the response to LC doesn't make it useless.

For GT's example to be a credible challenge to the food reward idea, he would have to provide a detailed before and after account of the diet of that culture. He has not provided that and I don't know where to find it myself.

Stephan, You are brilliant, and I - along with many here - am grateful for your ability to translate very complicated science into a "readable format" ;).

My interests lie in prevention of childhood obesity, and my main focus of research and program/product development is on the significant changes that have occurred in the toddler diet over the past 15 years. I have long believed that the transition from a bland puree-based infant diet to today’s highly palatable toddler diet (consisting of rotating ‘kid friendly’ meals and snacks) is the insidious pitfall that most parents fall into. However, in my research into fetal origins of obesity, I am now wondering if this is really just the spark to a fuse already established.

I was wondering if you had any thoughts on epigenetic mutations to the D2 receptor genes in the offspring of mothers who consumed a highly processed/palatable perinatal diet. I was most interested in hearing your thoughts on whether or not metabolic programming could be influenced through the fetus’s exposure to these highly palatable foods in humans.

It’s hard to deny the parallel trajectories that extreme obesity in children have had with the engineering and marketing of highly palatable foods. 20 years ago, extreme obesity in kids was considered rare, and often the result of a genetic anomaly or a metabolic condition or disease. Yet in the past 15 years, the rates of extreme obesity in children (defined as 200% IBW) have increased at such a fast rate that it is now its own classification (in fact, rates of extreme obesity in children has risen faster than the rates of childhood obesity).

I’d be curious for your thoughts, and the thoughts of the many intelligent bloggers on your posts. Thank you!

Thank you for your answer. I know the variety exists.I am afraid I am bias due to my experience. I personally saw how LC worked exactly the same for 7 people me included . I saw posts on the internet made about the negative LC experience and I trust the people who complained about it, I just never meet such person. It doesn't prove LC is better, but explains my prejudgment.

I was on a bland food diet as a child. Remember trying to steal a pickled tomato from the jar while mom was not looking.

I read your dismissal of the fat-mother-malnourished child combination in some earlier post and was not convinced because such examples exist all over the world in the groups of poor people living mostly on chip carbs .It is hard to imagine exactly the same past history in each case.

It is not necessary to overeat in order to be fat. Your theory is dealing with gluttons eating fast-food. They exists for sure, but it is a more narrow group of people than the group of people who can be helped by LC. Fat mothers in poor countries most probably eating low-reward food already.

I share your concern about the consumption of the food designed to produce compulsive eating because it causes disaster for public health. However, I look at it from the side because nor me, nor my family consume it. I also observed the rising propaganda of breakfast cereals, low-fat foods,juices, sugary yogurt-based drinks and rising obesity in Russia especially among children. Fast-food consumption is getting more popular there, not from the children, but from more affluent middle-class adults. For them it is trendy, modern food. They are getting fatter too, of course. People know that fast food is wrong. The more danger for the society is in the under-appreciation of the high-carb foods that are assumed to be healthy.Sorry for the long post, I just want to be understood.

I have enjoyed your blog over a year now; I wanted to thank you for your unselfish sharing of your thoughts. so, then, this appears on Bloomberg.com today....http://www.bloomberg.com/news/2011-11-02/fatty-foods-addictive-as-cocaine-in-growing-body-of-science.html

In regard to your comments about marijuana, I know anecdotally that its habitual users find it difficult to eat without it, and that if - for whatever reason - they suddenly stop taking it, they almost entirely lose their appetite and it takes a week or so for it to return to normal.

Im not academic, trained or particularly knowledgeable in the field of nutrition but have a few observations which I think may be relevant.

I believe that in some instances junk food can be low in palatability and low reward. Years ago I worked at an all night restaurant at an airport and ate pretty much nothing but junk food for nigh on 3 years. I put a bit of weight on to start with probably as I could eat a bacon sandwich or portion of chips whenever I wanted but soon my weight stabalised. Over time however the food became pretty bland and unappealing and I would often crave fresh fruit and veg as much as a regular person might crave a bag of crisps.

Another thing I have noticed is that amoungst many cultures fatness isnt necessarily considered a bad thing, being fat was a sign of wealth and health, if you were fat it meant you were a good hunter or your farm was doing well. Many of my elder relatives would be more shocked if you turned up a family reunion and had lost weight rather than put it on, usually weight loss was a sign that someone wasn't well.

About Me

I'm a writer and science consultant with a background in neuroscience and obesity research. I have a BS in biochemistry and a PhD in neurobiology. I'm the author of "The Hungry Brain: Outsmarting the Instincts That Make Us Overeat".

Copyright 2008-2017

Please feel free to reproduce the contents of this blog, on the condition that you:

1) Attribute the work to me

2) Provide a link to the page where you found it

3) Do not use it for commercial purposes

Financial disclosure

I am a co-creator of the Ideal Weight Program, and I receive revenue from the sale of this program.

In addition, I am registered as an Amazon affiliate. I may receive a small commission on the sale of some of the books I review, or other products sold through Amazon.

Disclaimer

This blog is a compilation of my opinions. It's not advice; it's information that you can take or leave as you please. I don't intend it to replace professional medical consultation or treatment. Your health is in your own hands.